INT141658

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Context Info
Confidence 0.69
First Reported 2006
Last Reported 2010
Negated 2
Speculated 2
Reported most in Body
Documents 51
Total Number 53
Disease Relevance 35.60
Pain Relevance 3.71

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

mitochondrion (Sod2) oxidoreductase activity (Sod2) mitochondrion organization (Sod2)
DNA binding (Sod2) response to stress (Sod2) cytoplasm (Sod2)
Anatomy Link Frequency
blood 12
liver 4
dorsal root ganglia 4
retina 2
spinal cord 2
Sod2 (Mus musculus)
Pain Link Frequency Relevance Heat
Eae 143 99.72 Very High Very High Very High
dorsal root ganglion 21 99.52 Very High Very High Very High
Spinal cord 13 99.28 Very High Very High Very High
imagery 510 98.30 Very High Very High Very High
cytokine 88 98.08 Very High Very High Very High
Central nervous system 173 96.88 Very High Very High Very High
diabetic neuropathy 21 96.68 Very High Very High Very High
Inflammation 108 95.96 Very High Very High Very High
Inflammatory response 45 92.96 High High
Potency 27 92.20 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 322 99.88 Very High Very High Very High
Stress 881 99.74 Very High Very High Very High
Hyperglycemia 1160 99.72 Very High Very High Very High
Diabetic Retinopathy 1 99.62 Very High Very High Very High
Disease 1514 99.60 Very High Very High Very High
Skin Cancer 7 99.52 Very High Very High Very High
Death 64 99.36 Very High Very High Very High
Neuropathic Pain 22 99.16 Very High Very High Very High
Injury 189 99.08 Very High Very High Very High
Ganglion Cysts 29 99.04 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
SOD2 overexpression reduces mitochondrial superoxide load.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2
1) Confidence 0.69 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2956689 Disease Relevance 1.02 Pain Relevance 0.12
Similarly, SOD2 overexpression in heart mitochondria improved mitochondrial respiration, protected heart morphology, and restored cardiac contractility of a diabetic heart [31].
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 in heart associated with diabetes mellitus
2) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.71 Pain Relevance 0.08
For example, SOD2 overexpression in primary dorsal root ganglion cultures or in mice protected cellular injury and prevented development of signs of diabetic neuropathy (DN) respectively [10].
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 in dorsal root ganglion associated with ganglion cysts, dorsal root ganglion, diabetic neuropathy and injury
3) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.31 Pain Relevance 0.10
Our results describe restoration of axonal transport rates following SOD2 overexpression in animal models, and although the model we use does not directly correlate with human disease, similar outcome may be possible in diabetic patients, provided optimization of timing, dosage and potency of antioxidant therapy used.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 associated with diabetes mellitus, disease and potency
4) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.14 Pain Relevance 0.08
In this study, we utilized two different animal models: (i) STZ-induced hyperglycemia mice and (ii) a heterozygotic SOD2 overexpressing STZ-treated hyperglycemia mice.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SOD2 associated with hyperglycemia
5) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 0.65 Pain Relevance 0.09
Last, we hypothesize that reduction of oxidative stress through the overexpression of SOD2 should ameliorate these effects.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 associated with stress
6) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.15 Pain Relevance 0.17
Whereas hyperglycemia-induced oxidative stress damages peripheral neurons, overexpression of SOD2 reduces the superoxide load and prevents hyperglycemia-induced cellular injury in dorsal root ganglia (DRG) cultures [10].
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 in dorsal root ganglia associated with stress, hyperglycemia and injury
7) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.39 Pain Relevance 0.06
Additionally, overexpression of SOD2 reduces symptoms of neuropathy in streptozotocin (STZ) treated C57Bl/6 mice [10].
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 associated with neuropathic pain
8) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.44 Pain Relevance 0.04
Furthermore, overexpression of SOD2 significantly prevented the development of retinopathy in mice by preventing retina from diabetes-induced oxidative damage [30].
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 in retina associated with diabetes mellitus and ocular toxicity (including many sub-types)
9) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.57 Pain Relevance 0.09
Recently, Munusamy and Mac-Millan-Crow [29] reported that overexpression of SOD2 prevented early stage hyperglycemia-induced mitochondrial injury in normal renal rat proximal tubular cells.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2 in proximal associated with hyperglycemia and injury
10) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.54 Pain Relevance 0.09
Upon SOD2 overexpression, the deficits in axonal transport recovered in association with restoration of levels of phosphorylated p38 MAPK and tau protein.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD2
11) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 0.88 Pain Relevance 0.09
T1-weighted MEMRI imaging was used to determine axonal transport rates post-streptozotocin injection in wildtype (WT) and superoxide dismutase 2 (SOD2) overexpressing C57Bl/6 mice.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SOD2 associated with imagery
12) Confidence 0.69 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2956689 Disease Relevance 0.98 Pain Relevance 0.12
Overexpression of SOD-2, and therefore reduction of mitochondrial superoxide, resulted in a recovery of the rCBF back to normal levels (Figure 1).
Positive_regulation (Overexpression) of Gene_expression (Overexpression) of SOD-2
13) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.52 Pain Relevance 0.10
This deficit was rescued with overexpression of SOD-2, indicating that mitochondrial superoxide plays a key role in the axonopathy associated with AD.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2 associated with disease
14) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.30 Pain Relevance 0.08
Utilizing the MRI methodology arterial spin labeling (ASL), we measured the regional cerebral blood flow (rCBF) in the cortex of Tg2576 mice with or without SOD-2 overexpression, at ages ranging from 4 to 16 months.
Neg (without) Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2 in blood associated with imagery
15) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.59 Pain Relevance 0.11
Using a novel dynamic MRI imaging technique, MEMRI, we measured in vivo axonal transport rates in the Tg2576 mice, with or without SOD-2 overexpression, at ages ranging from 4 to 16 months.
Neg (without) Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2 associated with imagery
16) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.22 Pain Relevance 0.10
Herein we have shown that reducing mitochondrial superoxide by SOD-2 overexpression ameliorated cerebral blood flow deficits and axonal transport deficits typically exhibited by Tg2576 mice.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2 in blood
17) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.12 Pain Relevance 0
Phosphorylation of tau is returned back to normal with SOD-2 overexpression, indicating that mitochondrial superoxide also affects axonal transport through tau dysfunction.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2
18) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.55 Pain Relevance 0.07
Moreover, overexpression of SOD-2 in the Tg2576 mice reduced the levels of phospho-eNOS back to those in wild-type mice (Figure 2), which corresponded with the recovered blood flow deficits in these same mice.


Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2 in blood
19) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.20 Pain Relevance 0.08
This increase was recovered back to wildtype levels upon SOD-2 overexpression, suggesting that mitochondrial superoxide contributes to tau pathology not only in the olfactory bulb, but also extends to the learning and memory centers of the brain.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD-2 in brain
20) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.38 Pain Relevance 0.09

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